scholarly journals Eicosanoids and Oxidative Stress in Diabetic Retinopathy

Antioxidants ◽  
2020 ◽  
Vol 9 (6) ◽  
pp. 520 ◽  
Author(s):  
Mong-Heng Wang ◽  
George Hsiao ◽  
Mohamed Al-Shabrawey
Keyword(s):  
Oxidative Stress ◽  
Diabetic Retinopathy ◽  
Renin Angiotensin System ◽  
Microvascular Dysfunction ◽  
Microvascular Damage ◽  
Angiotensin System ◽  
Ras Activation ◽  
Long Time ◽  
And Oxidative Stress

Oxidative stress is an important factor to cause the pathogenesis of diabetic retinopathy (DR) because the retina has high vascularization and long-time light exposition. Cyclooxygenase (COX), lipoxygenase (LOX), and cytochrome P450 (CYP) enzymes can convert arachidonic acid (AA) into eicosanoids, which are important lipid mediators to regulate DR development. COX-derived metabolites appear to be significant factors causative to oxidative stress and retinal microvascular dysfunction. Several elegant studies have unraveled the importance of LOX-derived eicosanoids, including LTs and HETEs, to oxidative stress and retinal microvascular dysfunction. The role of CYP eicosanoids in DR is yet to be explored. There is clear evidence that CYP-derived epoxyeicosatrienoic acids (EETs) have detrimental effects on the retina. Our recent study showed that the renin-angiotensin system (RAS) activation augments retinal soluble epoxide hydrolase (sEH), a crucial enzyme degrading EETs. Our findings suggest that EETs blockade can enhance the ability of RAS blockade to prevent or mitigate microvascular damage in DR. This review will focus on the critical information related the function of these eicosanoids in the retina, the interaction between eicosanoids and reactive oxygen species (ROS), and the involvement of eicosanoids in DR. We also identify potential targets for the treatment of DR.

scholarly journals Hyperactivated RAGE in Comorbidities as a Risk Factor for Severe COVID-19—The Role of RAGE-RAS Crosstalk

Biomolecules ◽  
2021 ◽  
Vol 11 (6) ◽  
pp. 876
Author(s):  
Sara Chiappalupi ◽  
Laura Salvadori ◽  
Rosario Donato ◽  
Francesca Riuzzi ◽  
Guglielmo Sorci
Keyword(s):  
Gene Polymorphisms ◽  
Renin Angiotensin System ◽  
Molecular Target ◽  
Advanced Glycation ◽  
Angiotensin System ◽  
Major Player ◽  
Glycation End Products ◽  
End Products ◽  
And Oxidative Stress

The receptor for advanced glycation-end products (RAGE) is a multiligand receptor with a role in inflammatory and pulmonary pathologies. Hyperactivation of RAGE by its ligands has been reported to sustain inflammation and oxidative stress in common comorbidities of severe COVID-19. RAGE is essential to the deleterious effects of the renin–angiotensin system (RAS), which participates in infection and multiorgan injury in COVID-19 patients. Thus, RAGE might be a major player in severe COVID-19, and appears to be a useful therapeutic molecular target in infections by SARS-CoV-2. The role of RAGE gene polymorphisms in predisposing patients to severe COVID-19 is discussed. 

Abstract 1375: Brain Renin Angiotensin Blockade Attenuates Cytokines and Oxidative Stress in the Paraventricular Nucleus of Hypothalamus and Decreases Sympathoexcitation in Heart Failure Rats

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Ying Ma ◽  
Yu-Ming Kang* ◽  
Zhi-Ming Yang ◽  
Joseph Francis*
Keyword(s):  
Oxidative Stress ◽  
Heart Failure ◽  
Paraventricular Nucleus ◽  
Cross Talk ◽  
Renin Angiotensin System ◽  
Heart Weight ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
The Brain ◽  
And Oxidative Stress

Introduction: Neurohumoral mechanisms play an important role in the pathophysiology of congestive heart failure (HF). Recent studies suggest that the brain renin angiotensin system (RAS) plays an important role in regulating body fluids and sympathetic drive in HF. In addition, it has been shown that there is cross talk between cytokines and RAS in cardiovascular disease. In this study we determined whether blockade of brain RAS attenuate inflammatory cytokines and oxidative stress in HF rats. Methods and Results: Adult male Sprague-Dawley rats were implanted with intracerebroventricular (ICV) cannulae and subjected to coronary artery ligation to induce HF and confirmed by echocardiography. Rats were treated with an angiotensin type 1 receptors (AT1-R) antagonist losartan (LOS, 20 μg/hr, ICV) or vehicle (VEH) for 4 weeks. At the end of the study, left ventricular (LV) function was measured by echocardiography and rats were sacrificed, and brain and plasma samples were collected for measurements of cytokines and superoxide using immunohistochemistry, Western blot and real time RT-PCR. HF rats induced significant increases in Nuclear Factor-kappaB (NF-κB) p50-positive neurons and activated microglia in the paraventricular nucleus (PVN) of hypothalamus, and TNF-α, IL-1β, IL-6 and NF-κB p50 in hypothalamus when compared with sham rats. These animals also had increased staining for dihydroethidium (DHE) and plasma levels of norepinephrine (NE), an indirect indicator of sympathetic activity. In contrast, ICV treatment with LOS attenuated cytokine expression and oxidative stress in the PVN and hypothalamus when compared with VEH treated HF rats. ICV treatment with LOS also reduced plasma NE levels, and proinflammatory cytokine, heart weight to body weight ratio with decreased LV end-diastolic pressure. Conclusions : These findings suggest the cross talk between the cytokines and renin angiotensin system within the brain contribute to sympatho-excitation in HF.

Abstract 314: Elevation of (pro)renin and Its Receptor in Preeclampsia: A Rat Model and Human Patients

Hypertension ◽  
2012 ◽  
Vol 60 (suppl_1) ◽  
Author(s):  
Mohammad N Uddin ◽  
Darijana Horvat ◽  
Russell E Fothergill ◽  
Kelsey R Kelso ◽  
Richard O Jones ◽  
...  
Keyword(s):  
Rat Model ◽  
Renin Angiotensin System ◽  
Placental Tissue ◽  
Pregnant Rats ◽  
Angiotensin System ◽  
Ras Activation ◽  
Kolmogorov Smirnov ◽  
Desoxycorticosterone Acetate ◽  
A Site

Preeclampsia (PreE), a syndrome manifesting with hypertension, proteinuria, and edema, is a leading cause of maternal and fetal morbidity and mortality. While preE triggers are likely many and elusive, the renin-angiotensin system (RAS) has been implicated in preE pathogenesis. However, there is no data showing involvement of (pro)renin and its receptor. We recruited 32 preE and 57 normal pregnant consenting patients. (Pro)renin levels were assayed in plasma samples using an ELISA kit. An established rat model of preE was used to evaluate the role of (pro)renin and its receptor in pathogenesis. We used normal pregnant rats (NP, n=10) and pregnant rats receiving weekly injections of desoxycorticosterone acetate and whose drinking water was replaced with 0.9% saline (PreE, n=10). The plasma and placental levels of (pro)renin were assayed by ELISA. The placental levels of (pro)renin receptor was measured by gel electrophoresis of the placental homogenate followed by detection with immunoblotting using anti-ATP6IP2 antibody. The ERK1/2 phosphorylation was analyzed by immunoblotting using antibodies to total and active ERK1/ERK2 in the placenta. The mean plasma (pro)renin of 0.27 ± 0.04 μg/mL in preE patients differ (p < 0.001 using Student’s t test) from 0.15 ± 0.05 μg/mL in those without preE. Both plasma and placental levels of (pro)renin were higher (p < 0.001 using Kolmogorov-Smirnov test) in PreE rats compared to NP (Plasma (pro)renin for NP:0.21 ± 0.04 and PreE:0.49 ± 0.09 pg/mL; placental (pro)renin for NP:152 ± 79 and PreE:302 ± 42 ng/g tissue). In addition to serving as a source of (pro)renin, the placenta is also a site for signaling as ERK1/2 phosphorylation is greater (p<0.05) in placental tissue of preE rats. These data show that circulatory and uteroplacental (pro)renin and its receptor are upregulated. Together with the upregulation of ERK1/2 phosphorylation in placenta of the rat model, there is now evidence of (pro)renin and its receptor associated novel RAS activation to play a role in preE pathogenesis through (pro)renin receptor-mediated detrimental cellular signaling at the placental boundary. This offers an opportunity for interventional treatments with signal inhibitors and interference with nonclassical (pro)renin activation of RAS.

scholarly journals Açaí (Euterpe oleracea Mart.) seed extract protects against hepatic steatosis and fibrosis in high-fat diet-fed mice: Role of local renin-angiotensin system, oxidative stress and inflammation

2020 ◽  
Vol 65 ◽  
pp. 103726 ◽  
Author(s):  
Matheus Henrique Romão ◽  
Graziele Freitas de Bem ◽  
Izabelle Barcellos Santos ◽  
Ricardo de Andrade Soares ◽  
Dayane Teixeira Ognibene ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Hepatic Steatosis ◽  
High Fat Diet ◽  
Renin Angiotensin System ◽  
Seed Extract ◽  
Euterpe Oleracea ◽  
High Fat ◽  
Angiotensin System ◽  
Euterpe Oleracea Mart

The Renin-Angiotensin System and the Cerebrovascular Diseases: Experimental and Clinical Evidence

2020 ◽  
Vol 27 (6) ◽  
pp. 463-475 ◽  
Author(s):  
Lucas M. Kangussu ◽  
Lucas Alexandre Santos Marzano ◽  
Cássio Ferraz Souza ◽  
Carolina Couy Dantas ◽  
Aline Silva Miranda ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Renin Angiotensin System ◽  
Cerebrovascular Diseases ◽  
Therapeutic Effects ◽  
Angiotensin System ◽  
Renin Angiotensin ◽  
Mas Receptor

Cerebrovascular Diseases (CVD) comprise a wide spectrum of disorders, all sharing an acquired or inherited alteration of the cerebral vasculature. CVD have been associated with important changes in systemic and tissue Renin-Angiotensin System (RAS). The aim of this review was to summarize and to discuss recent findings related to the modulation of RAS components in CVD. The role of RAS axes is more extensively studied in experimentally induced stroke. By means of AT1 receptors in the brain, Ang II hampers cerebral blood flow and causes tissue ischemia, inflammation, oxidative stress, cell damage and apoptosis. On the other hand, Ang-(1-7) by stimulating Mas receptor promotes angiogenesis in brain tissue, decreases oxidative stress, neuroinflammation, and improves cognition, cerebral blood flow, neuronal survival, learning and memory. In regard to clinical studies, treatment with Angiotensin Converting Enzyme (ACE) inhibitors and AT1 receptor antagonists exerts preventive and therapeutic effects on stroke. Besides stroke, studies support a similar role of RAS molecules also in traumatic brain injury and cerebral aneurysm. The literature supports a beneficial role for the alternative RAS axis in CVD. Further studies are necessary to investigate the therapeutic potential of ACE2 activators and/or Mas receptor agonists in patients with CVD.

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